Navab M, Berliner J A, Watson A D, Hama S Y, Territo M C, Lusis A J, Shih D M, Van Lenten B J, Frank J S, Demer L L, Edwards P A, Fogelman A M
Atherosclerosis Research Unit, School of Medicine, University of California at Los Angeles 90095-1736, USA.
Arterioscler Thromb Vasc Biol. 1996 Jul;16(7):831-42. doi: 10.1161/01.atv.16.7.831.
Recent data support the hypothesis that the fatty streak develops in response to specific phospholipids contained in LDL that become trapped in the artery wall and become oxidized as a result of exposure to the oxidative waste of the artery wall cells. The antioxidants present within both LDL and the microenvironments in which LDL is trapped function to prevent the formation of these biologically active, oxidized lipids. Enzymes associated with LDL and HDL (eg, platelet activating factor acetylhydrolase) or with HDL alone (eg, paraoxonase) destroy these biologically active lipids. The regulation and expression of these enzymes are determined genetically and are also significantly modified by environmental influences, including the acute-phase response or an atherogenic diet. The balance of these multiple factors leads to an induction or suppression of the inflammatory response in the artery wall and determines the clinical course.
脂肪条纹的形成是对低密度脂蛋白（LDL）中所含特定磷脂的反应，这些磷脂被困在动脉壁中，并因暴露于动脉壁细胞的氧化废物而被氧化。LDL以及LDL被困其中的微环境中存在的抗氧化剂具有防止这些具有生物活性的氧化脂质形成的作用。与LDL和高密度脂蛋白（HDL）相关的酶（如血小板活化因子乙酰水解酶）或仅与HDL相关的酶（如对氧磷酶）会破坏这些具有生物活性的脂质。这些酶的调节和表达由基因决定，也会受到环境影响的显著改变，包括急性期反应或致动脉粥样化饮食。这些多种因素的平衡导致动脉壁炎症反应的诱导或抑制，并决定临床病程。
